• BMB Reports
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• v.38 no.3
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• pp.300-306
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• 2005

Tamoxifen citrate is an anti-estrogenic drug used for the treatment of breast cancer. It showed a degree of hepatic carcinogenesis, when it used for long term as it can decrease the hexose monophosphate shunt and thereby increasing the incidence of oxidative stress in liver rat cells leading to liver injury. In this study, a model of liver injury in female rats was done by intraperitoneal injection of tamoxifen in a dose of 45 mg/kg body weight for 7 successive days. This model produced a state of oxidative stress accompanied with liver injury as noticed by significant declines in the antioxidant enzymes (glutathione-S-transferase, glutathione peroxidase and catalase) and reduced glutathione concomitant with significant elevations in TBARS (thiobarbituric acid reactive substance) and liver transaminases; sGPT (serum glutamate pyruvate transaminase) and sGOT (serum glutamate oxaloacetate transaminase) levels. The oral administration of dimethyl dimethoxy biphenyl dicarboxylate (DDB) in a dose of 200 mg/kg body weight daily for 10 successive days, resulted in alleviation of the oxidative stress status of tamoxifen-intoxicated liver injury in rats as observed by significant increments in the antioxidant enzymes (glutathione-S-transferase, glutathione peroxidase and catalase) and reduced glutathione concomitant with significant decrements in TBARS and liver transaminases; sGPT and sGOT levels. The administration of DDB before tamoxifen intoxication (as protection) is more little effective than its curative effect against tamoxifen-induced liver injury. The data obtained from this study speculated that DDB can mediate its biochemical effects through the enhancement of the antioxidant enzyme activities and reduced glutathione level as well as decreasing lipid peroxides.

• The Journal of Internal Korean Medicine
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• v.43 no.4
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• pp.643-655
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• 2022

Objective: To investigate the protective effects of Haeganjeon on a thioacetamide (TAA)-induced liver fibrosis mouse model and to determine the Haegan-jeon signaling pathway. Methods: Mice were randomly divided into 4 groups: Normal group (Nor), TAA-induced liver fibrosis group (Con), TAA-induced liver fibrosis group administered 50 mg/kg silymarin (S50), TAA-induced liver fibrosis group administered 200 mg/kg Haegan-jeon (H200). The liver fibrosis mouse model was established by intraperitoneal injection with TAA three times a week for 8 weeks. During the 8 weeks, mice were orally administered silymarin and Haegan-jeon every day. At the end of the study, serum was collected to measure the levels of AST, ALT, ammonia, and myeloperoxidase (MPO). Liver tissue was harvested and analyzed by western blotting and Masson's trichrome staining. Results: Administration of Haegan-jeon suppressed the increase in serum levels of AST, ALT, ammonia, and MPO due to TAA-induced liver fibrosis. Compared to the Con group, the H200 group showed increases in antioxidant-related factors (Nrf2, HO-1, catalase, and GPx-1/2) and decreases in inflammatory-related factors (NF-κB p65, p-IκB-α, Cox-2, iNOS, TNF-α, and IL-1β) in western blots. The H200 treatment inhibited the expression of α-SMA and Collagen I. Conclusions: Haegan-jeon showed a hepatoprotective effect induced by activation of antioxidant-related factors, such as Nrf2, and it regulated the inflammation response by suppression of NF-κB.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.385.2-385.2
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• 2002

Cornus officinalis has been used as protective drug for liver and kidney function. In order to evaluate the effect on renal function of Corni Fructus. We measured urine volume, chemical parameters(urea nitrogen. creatinine, uric acid). electrolytes($Na^{+}$, $K^{+}$, $Cl^{-}$) in serum and urine. Furosemide showed significant urine volume. serum and urine parameters, but Corni Fructus showed normal level parameters by dose increasing in rats.

• Korean Journal of Food Science and Technology
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• v.31 no.4
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• pp.1096-1100
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• 1999

The protective effect of Bifidobacterium breve K-110, K-111 and B. infantis K-525 on carbon tetrachloride induced hepatotoxicity in rats was investigated. Among them, B. infantis K-525 had the most potent hepatoprotective activity. It reduced serum aspartate aminotransferase and alanine aminotransferase levels to 51% and 80% of the $CCl_{4}-treated$ groups, respectively. In rat liver homogenate intoxificated with $CCl_{4}$, B. infantis K-525 inhibited in vitro as well as in vivo lipid peroxidation more than the other Bifidobacteria.

• Journal of Applied Biological Chemistry
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• v.61 no.4
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• pp.411-416
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• 2018

Chlorpyrifos (CPF) is one of the most heavily used organophosphate pesticides and is useful as an insecticide drug. However, CPF also causes toxic effects in nontarget organisms, including humans and animals. Jageum-Jung (JGJ) is a traditional oriental medicine, composed of five specific herbs with antioxidant and hepatoprotective properties, used for detoxification. In the present study, highly concentrated CPF was orally administrated to male Institute of Cancer Research mice to produce acute toxicity, and the protective effects of JGJ administration were investigated through statistical analysis of changes in body and organ weights and serum biochemical parameters. JGJ caused body and organ weights to recover and reduced the levels of serum biochemical parameters indicative of liver damage, such as glutamic oxalate transaminase, glutamic pyruvate transaminase, alkaline phosphatase, lactic dehydrogenase, urea, glucose, total cholesterol, and triglyceride, that had been increased by CPF treatment. Our results demonstrated that JGJ ameliorates the effects of acute chlorpyrifos-induced toxicity. Therefore, JGJ has the potential to be used as a traditional medicine to alleviate insecticide toxicity.

• Journal of the Korean Society of Food Science and Nutrition
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• v.23 no.5
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• pp.750-756
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• 1994

The effect of onion juice on ethanol -induced lipid peroxidation were studied were studied in rats. The contents of thiobarbituric acid (TBA) -reactants increased significantly in liver thanol(4ml/kg/day) administered -rats. The activities of serum alanine aminotransferase and alkaline phosphatase increased by ethanol administration compared with control group, but alterations of antioxidant enzymes activities in liver of ethanol administered rats were not significant vs control group. The glutathione contents in liver decreased by ethanol , whereas the glutathione level increased in ethanol and onion juice group compared with ethanol group. The contents of hepatic TBA-reactants and serum aminotrasnferase activity in ethanol group were reduced by onion juice administration. In these results, increased hepatic TBA-reactants of liver in ethanol group might be due to decreased glutathione contents in liver. Reduced glutathione (GSH) plays an important roles in the liver in several detoxification and the reduction of lipid peroxides. So the protective effects of onion juice on ethanol-induced increment of TBA-reactants may be due to the increament of lgutathions content. The glutathione depletion by ethanol was an important factor of ethanol-induced cell damage, and the prevention of onion juice to the glutathione depletion reduced by ethanol may be an important factor on the protection from ethanol-induced lipid perpxidation in rats.

• Nutrition Research and Practice
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• v.14 no.4
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• pp.309-321
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• 2020

BACKGROUND/OBJECTIVES: The present study aimed to evaluate the effects of folic acid supplementation in high-fructose-induced hepatic steatosis and clarify the underlying mechanism of folic acid supplementation. MATERIALS/METHODS: Male SD rats were fed control, 64% high-fructose diet, or 64% high-fructose diet with folic acid for eight weeks. Plasma glutamate-pyruvate transaminase, glutamate-oxaloacetate transaminase, lipid profiles, hepatic lipid content, S-adenosylmethionine (SAM), and S-adenosylhomocysteine (SAH) were measured. RESULTS: The HF diet significantly increased hepatic total lipid and triglyceride (TG) and decreased hepatic SAM, SAH, and SAM:SAH ratio. In rats fed a high fructose diet, folic acid supplementation significantly reduced hepatic TG, increased hepatic SAM, and alleviated hepatic steatosis. Moreover, folic acid supplementation in rats fed high fructose enhanced the levels of phosphorylated AMP-activated protein kinase (AMPK) and liver kinase B (LKB1) and inhibited phosphorylation of acetyl coenzyme A carboxylase (ACC) in the liver. CONCLUSIONS: These results suggest that the protective effect of folic acid supplementation in rats fed high fructose may include the activation of LKB1/AMPK/ACC and increased SAM in the liver, which inhibit hepatic lipogenesis, thus ameliorating hepatic steatosis. The present study may provide evidence for the beneficial effects of folic acid supplementation in the treatment of non-alcoholic fatty liver disease.

• Advances in Traditional Medicine
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• v.7 no.3
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• pp.311-320
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• 2007

The present study was designed to estimate the protective effect of (-) epigallocatechin gallate (EGCG) on ethanol-induced liver injury in rats. Chronic ethanol administration (6 g/kg/day ${\times}$ 60 days) caused liver damage that was manifested by the elevation of markers of liver dysfunction - aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, bilirubin and ${\gamma}$-glutamyl transferase in plasma and reduction in liver glycogen. The activities of alcohol metabolizing enzymes such as alcohol dehydrogenase and aldehyde dehydrogenase were found to be altered in alcohol-treated group. Ethanol administration resulted in the induction of cytochrome p450 and cytochrome-$b_{5}$ activities and reduction of cytochrome-c reductase and glutathione-S-transferase, a phase II drug metabolizing enzyme. Further, ethanol reduced the viability of isolated hepatocytes (ex vivo) as assessed by trypan blue exclusion test and induced hepatocyte apoptosis as assessed by propidium iodide staining. Treatment of alcoholic rats with EGCG restored the levels of markers of liver injury and mitigated the alterations in alcohol metabolizing and drug metabolizing enzymes and cyt-c-reductase. Increased hepatocyte viability and reduced apoptotic nuclei were observed in alcohol + EGCG-treated rats. These findings suggest that EGCG acts as a hepatoprotective agent against alcoholic liver injury.

• The Journal of Internal Korean Medicine
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• v.32 no.4
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• pp.550-564
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• 2011

Objectives : Oxidative stress seems to play a major role in mechanisms by which ethanol causes liver injury. Previous studies have shown that treatment with Yinjinchunggan-tang (Yinchenqinggan-tang, YJCGT) has protective effects on alcoholic liver disease. The aim of this study was to investigate the protective effects of YJCGT on alcohol-induced oxidative stress. Materials and Methods : In vitro, we evaluated the inhibitory activities of YJCHT on DPPH(1,1-diphenyl-2-picryl-hydrazyl), xanthine oxidase, trypsin, and hyaluronidase. In a cell culture model, we measured cell viability and proliferation, and the activities of superoxide dismutase (SOD), and catalase (CAT) after YJCGT treatment in C34 and E47 cell lines, and HepG2 cells transfected with/ without cytochrome P450IIE1 (CYP2E1) gene. In vivo, we estimated serum level of hepatic biochemical markers, and alcohol concentration in the blood. Results : YJCGT showed significant free radical scavenging activity against DPPH and xanthine oxidase and decreased hyaluronidase activity effectively in vitro. YJCGT also increased cell viability, and proliferation in C34 and in E47 cell lines, and increased activities of superoxide dismutase, and catalase in C34 and in E47 cell lines. YJCGT reduced serum AST, LDH, and total cholesterol level in some of the results, and reduced blood alcohol concentration in vivo, as well. Conclusions : This study suggests that YJCGT has protective effects on oxidative stress by inhibiting alcohol-induced suppression of antioxidant enzyme activities.

• Journal of Environmental Health Sciences
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• v.32 no.3
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• pp.235-239
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• 2006

Cichorium intybus (Compositae) has been used for fevers, dyspepsia, headache and jaundice, as a demulcent. Also, it has relaxation effects and relief effects against coffee and teas, and is widely used as food. We investigated anti-lipid peroxidative effects and liver protective activity on $CCl_4$ induced lipid peroxidation and hepatotoxicity in rats. MeOH Ex. enhanced the inhibition of anti-lipid peroxidative effects in liver lipid. In chemical parameters obtained from serum analysis, MeOH Ex. revealed significant decrease on hepatotoxicity. The results were as follows; 1. The inhibitory effects of lipid peroxidation were shown in accordance with the increase of samples' concentration level. 2. In chemical parameters obtained from serum analysis, the activities of GOT, GPT, AlP were restored to near the normal level. The contents of cholesterol and BUN showed inhibitory effects with valence. 3. The weights of liver and spleen were not able to restore to the normal level. But on a general level, they were reduced more than the control group.